Surrey and Sussex Healthcare NHS Trust East Surrey Hospital Regional weekly PA Teaching Program Rheumatoid Arthritis(RA) - MBBS MRCSEd Lead T&O SHO

Surrey and Sussex Healthcare NHS Trust
          East Surrey Hospital
 Regional weekly PA Teaching Program

 Rheumatoid Arthritis(RA)
 Presented by :
                  Dr.Eltayeb Shammeseldin
                       MBBS MRCSEd
                      Lead T&O SHO

                        10.3.2021

Introduction
 Commonest Chronic inflammatory joint
  disease
 1-3%prevelance
 40s-50s of age
 F:M 3-4:1
 Commoner in Caucasian in N. America
  and Europe, but it is everywhere

Etiopathogenesis theories
1.   Genetic susceptibility:
    1st degree relative of RA pt
    HLADR4 +ve in 70% of RA pt
2.   Autoimmune response:
    Antigen attracted to synovium?
     Presented to APC(B-cell with HLADR4)
    Type 4 reaction=chronic IFN(T-cell)
    Type 3 reaction=(anti-CCP Ab
     +R.F(anti-IgG Ab))

Etiopathogenesis theories
3.   Chronic synovitis(joints&tendon
     sheaths)=(cytokines(TNF,IL-1&IL-
     6)+Ab/Ag complexes,PGs)=destruction,
     granulation tissue,fibrosis
4.   Systemic involvement with Chronic IFN
     process
    Every organ involvement in different
     pace,not a one type process

RA pathological stages
1. Pre-clinical(years earlier)=no S&S,high
   CRP&ESR and RF present
2. Synovitis=acute IFN,joint mobile,not stiff
   (potentially reversible)
3. Destruction=chronic IFN destroy by :
 WCC +osteoclasts enzs
 Vascular and pannus invasion(granulation)
 Joint destruction+tendon rupture
4. Deformity =due to joint destruction +tendon
   rupture+ capsule laxity+

Extra-articular lesions pathology
1. Rheumatoid nodules=non-caseating
   necrotic subcutaneous granuloma over
   bony prominences, tendon(trigger),
   synovium,sclera,viscera(lung,kidey,GI
   ,heart)
2. LNs+splenomegaly(cells hyperactivity)
3. Vasculitis=nail infarction,MI
4. Myopathy or C1/C2 sublux,spine # or
   Cord compression
5. Peripheral neuropathy or nerve
   compression(CTS)

Clinical features
 Mostly insidious over months, but
  sometimes acute
 Early:
1. Symmetrical bilateral PIP
    arthritis/stiffness
2. Tiredess,muscleache,wt
    loss,unwellness
3. Early morning stiffness>30min
4. Spread to
    wrist>feet>knee>shoulder
5. Tender swollen joints, thick
    tendons (EPL,FDP,FDS),but no
    deformity, no restricted ROM

Clinical features
 Late:
1. Deformity, stiffness,
   dull ache pain,
   decrease ROM
2. Valgus knees&feet
                           &finger
3. Claw toes
4. Volar radial wrist
   displacement
5. 30%painfull/stiff
   neck

Clinical features
 Advanced:
 Late stage+extra-
  articular features
 In 25% of cases but
  pathonomoic

Investigations
    Bloods:
1.     FBC(normo
       normo,why?)
2.     ESR,CRP
3.     ANA +Ve in 30%,R.F
       80%=not specific or
       senstive
4.     Anti-CCP specific

     XRs:
     Early=swelling+peri-
      articular OP
     Late=decrease joint
      space+bone erosions

Investigations+Diagnosis
 US/MRI=for early ∆ of synovitis
 Synovial biopsy=not specific histo to RA

   ∆=clinical features>6/52 + blood results

 If u find RA, search for other autoimmune
 IDDM,Hashimoto’s, pernicious anemia
  anemia, Addison’s ,ITP,MG,SLE,PBC..etc

Differential diagnosis
1. Psoriasis=skin lesions+DIP
2. SLE=slap cheeks+lungs,ANCA
3. AS=SIJ+bamboo spine,seronegative
4. Reiter’s=urethritis,colitis,conjunctivitis
5. Polyarticular gout=crystals,tophi Histo.
6. Peudogout=chondrocalcinosis+crystals
7. Sarcoidosis=hilar LNs,high ACE,erthyma
   nodosum
8. Lyme disease=endemic areas,tics,serology

Differential diagnosis
9.  PMR=pelic/pectrol girdle,respond to low
    steriods,risks of GCA
10. Polyarticular OA=DIP&WB joints,there
    is osteophytes
 RA can do 2nd OA features,but no
    osteophytes

Rx(no CURE!!)
1.   Immediate IFN control by high dose
     prednislone and taper it
2.   Immediate DMARDs start to maintain
     control(single or combined)
    MTX or leflunomide +sulfasalazine or
     hydroxycholorquine
    If fail=biological TNF inhibitors(TFNI)=
     infliximab,etanercept,adalimumab

Rx(no CURE!!)
3.   Orthotics+physio
4.   Surgery=for pain,deformity,dysfunction
    Synvectmy,osteotomy,stabilization
    Tendon repair or transfer
    Arthroplasty,arthrodesis
    Need plan to stop/resume MTX and
     TFNI peri-operatively to help wound
     healing, in liaise with rheumatologist

Prognosis
 Worse with:
1. Female, younger age
2. High ESR,CRP, positive RF&anti-CCP
3. Bone erosions on first presentation
4. Extra-articular features presence
 Outcome:
 60% wax/wane,10%improves,
 10% deteriorates in 5 yrs
 10% becomes disabled

Complications
1.   Deformity
2.   Joint rupture
3.   Muscle weakness
4.   Septic arthritis
5.   Spinal cord compression
6.   Vasculitis and MI
7.   Amyloidosis and nephrotic syndrome
8.   Death,mostly by IHD

THANK YOU

QUESTIONS ARE
 WELCOMED,
 BEFORE BEEN
 QUESTIONED

Question1
What is the commonest gene related to RA?
1. HLA DR1
2. HLA B27
3. HLA DR4
4. HLA DQ2

Question 2
What is the least joint to be affected by RA?
1. PIPJ
2. Carporadial joint
3. Thumb IPJ
4. Hip

Question 4
What is the best blood test to diagnose RA?
1. RF
2. Anti-CCP
3. SMA
4. c-ANCA

Question 5
What is rheumatoid factor?
1. Anti-IgM antibodies
2. Anti-IgG antibodies
3. Anti-smooth muscle antibodies
4. Anti-T cell antibodies